European Journal of Cardiovascular Medicine

Background and Global Burden of Early-Onset CAD

Coronary artery disease (CAD) remains the leading cause of death worldwide, responsible for an estimated 17.9 million deaths annually, accounting for 32% of all global mortality [1]. Traditionally, CAD has been considered a disease of middle-aged and elderly populations; however, recent decades have witnessed a troubling rise in early-onset CAD, defined as CAD presenting before the age of 45 years in men and 55 years in women [2]. Epidemiological data reveal that 5–15% of all CAD cases now occur in young adults. This figure has remained steady or even increased in specific populations despite advances in cardiovascular prevention and treatment [3].

The emergence of CAD in young adults is particularly alarming due to its disproportionate socioeconomic impact. Individuals in this age group are typically in their most productive years, and the onset of CAD leads to premature morbidity, disability, loss of income, and increased healthcare costs [4]. Moreover, premature CAD often presents as acute coronary syndromes (ACS) or sudden cardiac death, frequently in individuals with few warning symptoms, making prevention and early detection a critical public health priority [5].

Definitions and Clinical Significance

Studies define early-onset CAD in varying ways. Most commonly, it refers to CAD diagnosed before age 45 in men and 55 in women, though some studies have used even stricter cutoffs (≤40 years) [6]. The significance of early-onset CAD lies not only in its epidemiology but also in its unique clinical, angiographic, and pathophysiological characteristics. Compared to older patients, younger adults more often present with single-vessel disease, soft plaques, and plaque rupture rather than calcified atherosclerosis [7]. Additionally, lifestyle-related factors such as smoking, sedentary behavior, and substance abuse are disproportionately represented in this group [8].

Notably, while short-term prognosis after an event is often favorable due to fewer comorbidities, long-term outcomes remain concerning, with high recurrence rates and poor adherence to secondary prevention [9]. This highlights the dual challenge of addressing both immediate management and sustained risk reduction in young adults with CAD.

Traditional Risk Factors

The risk factor profile of young adults with CAD reflects both overlaps and distinctions with older populations. Traditional cardiovascular risk factors—including smoking, hypertension, diabetes mellitus, dyslipidemia, and obesity—remain central contributors [10]. Smoking, in particular, is implicated in up to 60% of myocardial infarctions in young men, making it the single strongest modifiable risk factor in this age group [11]. Dyslipidemia, particularly low high-density lipoprotein (HDL) and elevated triglycerides, is also strongly associated with early-onset CAD, often reflecting metabolic syndrome [12].

Non-Traditional Risk Factors

Non-traditional factors have actually gained more recognition. They are definitely becoming important in research. Genetic factors like family history of high cholesterol, high lipoprotein(a) levels, and specific gene changes regarding apolipoproteins and inflammation genes contribute significantly [13]. 

Mental stress, depression, and anxiety are strongly linked with early heart disease, showing the connection between mental health and heart problems [14]. This highlights the significant role that psychological factors play in the development of cardiovascular risk and disease. Further, substance abuse, particularly cocaine and cannabis, itself contributes to ACS among young adults [15].

We are seeing new research that suggests body inflammation, as measured by hs-CRP and IL-6 tests, may be the primary cause of this problem. This finding can help doctors develop more effective prevention methods using only these blood markers.

Geographic and Sex-Based Variations

Geographic location and sex differences further influence disease patterns. The condition itself shows different rates across regions and between males and females.

We are observing that early-onset CAD manifests differently in various countries. The symptoms and their frequency vary worldwide. In rich countries, smoking has surely decreased, and blood pressure control has improved, which has kept heart disease rates stable. Moreover, in low- and middle-income countries, urban living, altered food habits, and reduced physical activity have led to an increase in heart disease cases [17]. South Asian people have much higher rates of early heart disease. This is due to the prevalence of genetic factors, insulin issues, and metabolic syndrome in this population [18].

Sex-based differences are also evident. Although early-onset CAD is more common in men, women present with more comorbidities (such as diabetes and autoimmune conditions) and have worse long-term outcomes [19]. Furthermore, delays in diagnosis and under-recognition of cardiovascular risk in young women contribute to disparities in management and prognosis [20].

Pathophysiology of Early-Onset CAD

Basically, CAD in young adults happens the same way through fast atherosclerosis and weak plaques. According to studies, younger patients have more lipid-rich plaques with thin caps that are more likely to rupture, leading to heart disease, compared to older patients [21]. These lesions actually have less calcium, which definitely suggests that factors beyond simple artery narrowing contribute to acute events. Inflammation, blood vessel problems, and clotting issues surely play key roles in this situation [22]. Moreover, these three factors work together to create serious health complications.

Basically, genetic changes in LDL receptor genes, PCSK9 variations, and microRNA alterations are the same factors that cause early plaque formation and make plaques unstable [23]. We observe that knowing these mechanisms is essential for creating targeted treatments and prevention methods.

Clinical Presentation and Outcomes

Early-onset CAD most frequently presents as acute coronary syndromes, with ST-elevation myocardial infarction (STEMI) being the most common subtype [24]. Regarding the presentation, these patients usually come with sudden, severe heart problems. We are seeing that stable angina is not very common in this group alone. As per medical studies, sudden cardiac death is more common in young men regarding silent heart disease cases. This often happens as the first sign when the heart problem was not diagnosed earlier.

Despite better short-term recovery due to fewer comorbidities, the lifetime burden of recurrent events, reduced quality of life, and socioeconomic loss is substantial.

Rationale for the Present Review

Despite the recognition of early-onset CAD as a distinct clinical entity, current literature remains fragmented. Previous reviews have primarily focused on traditional risk factors, without fully integrating genetic, psychosocial, and regional determinants. There is also limited synthesis of angiographic and long-term prognostic data. This systematic review aims to fill these gaps by:

1. Synthesizing epidemiological evidence on the prevalence and incidence of early-onset CAD.
2. Examining the full spectrum of traditional and non-traditional risk factors.
3. Describing clinical and angiographic characteristics unique to young adults.
4. Analyzing outcomes and identifying knowledge gaps to inform future research.

By addressing these areas, this review contributes to the understanding of early-onset CAD and lays the groundwork for precision-based prevention and intervention strategies in young adults.

Changing Epidemiological Trends

In earlier decades, CAD in young adults was considered rare; however, global epidemiological trends now highlight a shift toward earlier disease onset [1,2]. In high-income countries, while overall cardiovascular mortality has declined, rates of acute myocardial infarction (AMI) in individuals younger than 45 years have shown slight improvement [3]. In fact, registry data from the United States and Europe demonstrate that nearly one in eight hospital admissions for AMI now occurs in adults under 45, with many lacking a prior diagnosis of cardiovascular disease [4]. By contrast, in South Asia, the Middle East, and parts of Africa, the prevalence of early-onset CAD is substantially higher, underscoring the combined role of genetic susceptibility and rapid lifestyle transitions [5].

Lifestyle and Behavioral Determinants

According to studies, lifestyle risk factors are more prevalent in young CAD patients in terms of their health conditions. Tobacco use itself, including smoking and smokeless forms, remains the most consistent and modifiable risk factor [6]. Further research confirms this as the primary preventable cause. Also, in some areas, we are seeing that more than 70% of young men who get heart attacks are only active smokers. Emerging patterns also highlight the role of e-cigarettes and vaping, whose long-term cardiovascular risks are still under investigation [7].

We are seeing obesity and lack of physical activity rising very fast among young adults only, following the same pattern as metabolic syndrome worldwide. Sitting too much, along with more screen time and bad eating habits with processed foods and harmful fats, leads to early heart vessel damage [8]. Regarding dietary patterns, the consumption of refined sugars and trans fats exacerbates this problem. Alcohol and drugs like cocaine, amphetamines, and cannabis further worsen coronary blood vessel spasm and clot formation. This process itself can trigger heart attacks in healthy people [9].

Psychosocial and Socioeconomic Influences

Chronic psychosocial stress, depression, and anxiety disorders are increasingly recognized as independent risk factors for premature CAD [10]

Young adults face unique stressors—academic competition, job insecurity, and family responsibilities—that may exacerbate autonomic imbalance and pro-inflammatory states. Furthermore, poor economic conditions, limited access to healthcare, and a lack of health knowledge often delay diagnosis and treatment [11]. Basically, these factors show that CAD follows the same biopsychosocial pattern where mental health and social conditions significantly affect disease risk.

Genetic and Familial Contributions

While lifestyle factors dominate, genetic predisposition plays a significantly larger role in early-onset CAD compared to older populations [12]. Familial hypercholesterolemia (FH), characterized by LDL receptor mutations, accounts for up to 10% of premature CAD cases in some cohorts [13]. Elevated lipoprotein(a) [Lp(a)], a genetically determined lipoprotein, is also strongly implicated and is particularly prevalent in South Asian populations [14]. Genome-wide association studies (GWAS) have identified variants in loci such as 9p21, APOE, and PCSK9, further linking heritable traits to early disease onset [15]. Recognizing these familial patterns underscores the importance of cascade screening, where family members of affected patients undergo early risk stratification.

Sex Differences in Presentation and Outcomes

Although men comprise the majority of early-onset CAD cases, women present unique challenges. Women frequently exhibit non-obstructive CAD, microvascular dysfunction, and atypical symptoms, leading to underdiagnosis and delayed treatment [16]. Hormonal influences, pregnancy-related complications (e.g., preeclampsia, gestational diabetes), and higher prevalence of autoimmune disorders further contribute to cardiovascular risk in young women [17]. Alarmingly, mortality following an acute event is often higher in women than men, reflecting both biological and healthcare delivery disparities [18].

Angiographic and Pathological Features

Coronary angiography in young patients further shows single-vessel disease, with the left anterior descending artery (LAD) itself being most commonly affected [19]. Older adults surely have calcified atherosclerosis, but younger patients typically show soft, lipid-rich plaques. Moreover, these soft plaques are more prone to rupture and thrombosis [20]. This explains why we are seeing more cases of STEMI heart attacks only, not the long-term chest pain problems. Pathological studies confirm higher rates of plaque erosion and thrombus formation, highlighting the importance of pro-thrombotic states in premature CAD [21].

Health System and Preventive Gaps

A critical issue in early-onset CAD is the under-recognition of risk by both clinicians and patients.

A major problem in early heart disease is that doctors and patients actually don't recognize the risk well enough. This definitely leads to missing important warning signs. Young adults actually get fewer heart check-ups, and doctors definitely think they have low heart risk because of their age [22]. According to clinical observations, this results in missed opportunities for early treatment interventions. Young adults actually show poor follow-up with lifestyle changes and pharmacotherapy, including statins and antiplatelets [23]. They definitely do not stick to their treatment plans properly. Young people actually face barriers like no insurance, poor health knowledge, and cultural beliefs that heart disease only affects older adults. Moreover, as per clinical requirements, addressing these system gaps is essential for reducing repeat events and death rates.

Need for Precision Medicine and Public Health Integration

The heterogeneity of early-onset CAD highlights the need for a precision medicine approach. Genetic screening, biomarker profiling, and personalized risk calculators could improve early detection. Simultaneously, public health initiatives—such as anti-smoking campaigns targeting schools and colleges, workplace wellness programs, and community-based interventions—are essential for population-level prevention [24]. A dual approach that combines individualized care with broad preventive strategies is most likely to curb the rising burden of CAD in young adults.

Protocol and Reporting

This systematic review was conducted following the PRISMA 2020 guidelines for transparent reporting of systematic reviews and meta-analyses [25]. The protocol was designed in advance to minimize bias and clearly defined objectives, eligibility criteria, search strategies, and methods for data extraction and synthesis.

Literature Search Strategy

A comprehensive search was carried out in PubMed, Scopus, and Web of Science up to June 2025. Search terms included a combination of Medical Subject Headings (MeSH) and free-text keywords:

• “early-onset coronary artery disease”,
• “premature CAD”,
• “young adults and acute coronary syndrome”,
• “premature myocardial infarction”,
• “genetic risk factors in CAD”.

Boolean operators AND/OR were used to refine results, and search strategies were tailored for each database [26]. Additionally, manual searches of reference lists from relevant articles were performed to ensure completeness.

Eligibility Criteria

• Inclusion Criteria:
• Human studies of young adults (men <45 years old; women <55 years old) with angiographically or clinically confirmed CAD.
• Studies reporting epidemiology, risk factors, angiographic features, clinical outcomes, or preventive strategies.
• Peer-reviewed articles published in English.
• Exclusion Criteria:
• Case reports, case series with fewer than 10 patients, conference abstracts, editorials, or reviews without primary data.
• Studies lacking stratification by age to distinguish early-onset CAD.
• Non-English language publications [27].

Study Selection Process

Two reviewers independently screened all titles and abstracts for eligibility. They retrieved full-text versions of potentially relevant articles. Discrepancies were resolved by consensus or by consulting a third reviewer. In total, 60 studies met the inclusion criteria [28].

Data Extraction

A standardized data extraction form was used to ensure uniformity. Extracted data included:

• Study characteristics: author, year, country, study design, and sample size.
• Population characteristics: demographics, risk factor distribution, and comorbidities.
• Clinical data: presentation (stable angina, STEMI, NSTEMI, sudden cardiac death).
• Angiographic findings: number of vessels involved, lesion type, plaque morphology.
• Outcomes: short-term and long-term prognosis, recurrence, mortality, and adherence to secondary prevention.

Data were cross-checked by two reviewers for accuracy [29].

Quality Assessment

The methodological quality of studies was assessed using validated tools:

• Randomized Controlled Trials (RCTs): Cochrane Risk of Bias Tool 2.0.
• Observational Cohort and Case-Control Studies: Newcastle–Ottawa Scale (NOS).
• Registry and Survey-Based Analyses: assessed for sample size, representativeness, and completeness of outcome reporting.

Studies at high risk of bias were included but analyzed cautiously, with their limitations noted in the narrative synthesis [30].

Data Synthesis

Due to heterogeneity in populations, definitions, and outcomes across studies, a qualitative synthesis was performed. Epidemiological data and risk factor prevalence were summarized narratively. Where possible, prevalence ranges and pooled percentages were reported descriptively. A meta-analysis was not conducted because of variations in methodology, sample size, and reporting outcomes.

PRISMA Flow Summary

Overview of Included Studies

We found that only 60 studies met our criteria after review, and these studies originated from various regions, including North America, Europe, South Asia, the Middle East, and Africa. Further, these studies surely included population-based registries, case-control analyses, cohort studies, and interventional trials. Moreover, we used all these different research methods to gather comprehensive data. According to the studies, sample sizes ranged from small hospital groups with fewer than 100 patients to large multi-country registries involving several thousand people. Collectively, the studies provided a comprehensive view of epidemiology, risk factor clustering, clinical presentations, angiographic patterns, and outcomes of early-onset CAD [31].

Epidemiology and Demographics

The proportion of CAD in young adults varied across regions, ranging from 5–15% of total CAD burden [32]. Further studies show regional differences in this distribution. Basically, men made up 70-85% of early-onset cases, but women showed higher numbers in South Asian and Middle Eastern groups, which is the same pattern seen across different regions [33]. We observed that South Asian people get heart disease almost ten years earlier than Western people, and the disease is only more severe in them [34].

Basically, poor and middle-income countries saw more cases due to city living and lifestyle changes, while rich countries had the same rates but with more obesity and metabolic problems [35].

Risk Factor Distribution

Traditional Risk Factors

• Smoking: Present in up to 60–70% of young men with myocardial infarction, making it the single most substantial risk factor [36].
• Dyslipidemia: Elevated LDL and triglycerides with low HDL were common, often linked to poor dietary habits.
• Hypertension and Diabetes: Less prevalent than in older CAD, but early-onset diabetes was strongly associated with aggressive disease.
• Obesity/Metabolic Syndrome: Increasingly recognized in Western and South Asian cohorts [37].

Non-Traditional Risk Factors

• Genetic Factors: Familial hypercholesterolemia and elevated lipoprotein(a) were disproportionately represented [38].
• Substance Use: Cocaine and cannabis use were reported in up to 10–20% of young ACS cases in certain registries.
• Psychosocial Stress: High prevalence of depression, anxiety, and chronic stress contributed significantly [39].
• Autoimmune Diseases: Particularly in women, autoimmune disorders such as systemic lupus erythematosus increase CAD risk [40].

Clinical Presentation

The most common presentation was acute coronary syndrome, especially ST-elevation myocardial infarction (STEMI) [41].

• Stable angina was rare.
• NSTEMI and unstable angina were reported less frequently compared to older adults.
• Sudden cardiac death was disproportionately represented in young men, often due to undiagnosed CAD [42].

Young patients were also more likely to present late to healthcare facilities, with delayed diagnosis attributed to low suspicion by clinicians and patients themselves.

Angiographic Features

Distinct angiographic patterns were observed:

• Single-vessel disease (SVD) predominated, affecting 50–60% of cases, with the left anterior descending artery (LAD) most frequently involved [43].
• Multi-vessel disease was less common but correlated with diabetes and metabolic syndrome.
• Lesions were more likely to be soft plaques, prone to rupture and thrombosis, rather than calcified stenoses typically seen in older CAD patients [44].
• Some patients demonstrated angiographically normal coronaries despite myocardial infarction, suggesting vasospasm or thrombosis as the primary mechanism.

Short- and Long-Term Outcomes

• Short-term prognosis: Young patients generally had lower in-hospital mortality compared to older adults due to fewer comorbidities and preserved ventricular function.
• Long-term outcomes: Despite good early survival, recurrence rates of events were high, particularly in smokers and those with poor medication adherence.
• Secondary prevention gaps: Statin and antiplatelet use were suboptimal, with adherence rates often below 60% one year post-event [45].
• Quality of life impact: Studies documented significant psychosocial consequences, including depression, unemployment, and financial strain.

Regional and Sex-Based Variations

• South Asians: Younger age of onset, higher prevalence of diabetes and metabolic syndrome, and more severe angiographic disease.
• Western Populations: Higher prevalence of obesity and smoking-related CAD.
• Women: More likely to present with atypical symptoms, non-obstructive CAD, and microvascular dysfunction, leading to delayed treatment and worse long-term outcomes.

Synthesis of Key Findings

Key Takeaways

1. Early-onset CAD in young adults is a global health concern with distinct patterns.
2. Lifestyle determinants (smoking, obesity, substance abuse) remain dominant drivers, but genetic predispositions play a stronger role compared to older populations.
3. Clinical presentations are typically acute and severe, with angiographic evidence of vulnerable plaques rather than stable calcified lesions.
4. Despite better short-term survival rates, long-term recurrence rates remain significant due to poor adherence to secondary prevention measures.
5. Regional and sex-based variations highlight the need for personalized preventive and therapeutic strategies.

General Overview of Findings

This review demonstrates that early-onset CAD is a distinct clinical and epidemiological entity. Across 60 included studies, several consistent features emerged: (1) higher prevalence of traditional risk factors such as smoking, dyslipidemia, and early-onset diabetes; (2) an increasing role of non-traditional contributors such as genetics, psychosocial stress, and substance abuse; (3) a dominant presentation with acute coronary syndromes (mostly STEMI); and (4) angiographic profiles showing single-vessel disease and soft plaques prone to rupture rather than calcified stenosis. While short-term prognosis is relatively favorable due to fewer comorbidities, long-term recurrence and mortality are significant due to poor adherence to secondary prevention [46].

Risk Factor Patterns in Young Adults

Young CAD patients actually show clustering of smoking, obesity, dyslipidemia, and sedentary lifestyles. This definitely highlights a preventable component in these cases. Smoking actually emerged as the strongest factor and was definitely involved in more than half of all premature myocardial infarctions [47]. This is consistent with evidence showing that smoking promotes endothelial dysfunction, oxidative stress, and pro-thrombotic states, all of which accelerate atherogenesis in younger vessels.

On the other hand, genetic factors such as familial hypercholesterolemia (FH) and high lipoprotein(a) levels play a larger role, according to studies, in older patients [48]. Regarding genetic contributions, these have more impact in younger cases. As per some registries, FH was found in up to 10% of early-onset CAD cases. This shows FH is a major cause of heart disease in young people. We are seeing that these results indicate families need screening tests for all members, allowing doctors to help at-risk relatives early. This approach is only effective when we check the whole family together.

Clinical Presentation: Why STEMI Dominates

The predominance of STEMI among young adults is linked to the pathophysiology of vulnerable plaques. We are seeing that STEMI is more common in young adults only because of unstable plaques that can break easily. Essentially, younger patients have soft, fat-rich plaques with thin covers that rupture easily, leading to the formation of similar blood clots [49]. Older patients surely have stable, calcified plaques that cause chronic angina. Moreover, these plaques develop slowly over time and create long-lasting chest pain. Further, this explains why acute coronary syndromes themselves are the main feature of early-onset CAD, rather than stable presentations. Sudden heart problems are the same serious issue that needs immediate medical attention.

ac death is also more common in this age group, often as the first manifestation of disease.

Angiographic Features and Pathophysiological Insights

Angiographic studies consistently demonstrate single-vessel disease (SVD) in 50–60% of young CAD patients, with the LAD artery most frequently affected [50]. This contrasts with multi-vessel disease observed in older patients. Pathological studies confirm higher rates of plaque erosion and fresh thrombus formation, emphasizing the dynamic, thrombotic nature of CAD in young adults [51]. These differences have important therapeutic implications, as plaque stabilization and anti-thrombotic therapy may be particularly relevant in this population.

Prognosis and Secondary Prevention Gaps

Although in-hospital mortality is lower for younger CAD patients due to preserved cardiac function, long-term outcomes remain concerning. Recurrence rates are high, particularly in smokers, patients with diabetes, and those with genetic dyslipidemias [52]. A recurring theme across studies is the poor adherence to secondary prevention. Statin discontinuation rates approach 40% within the first year, and antiplatelet non-adherence is also common [53]. Psychosocial factors, lack of awareness, and financial barriers contribute to these gaps. This underscores the importance of structured rehabilitation programs and patient education tailored to younger populations.

Regional and Sex-Based Variations

The review confirms striking regional disparities. South Asians experience CAD nearly a decade earlier, often with more severe disease and higher rates of diabetes [54]. These differences are partly genetic but also reflect environmental exposures, including diets high in refined carbohydrates and lower levels of physical activity. Western populations, by contrast, show a higher prevalence of obesity and smoking-driven CAD.

Sex-based differences are equally significant. Women with early-onset CAD often present with non-obstructive disease, microvascular dysfunction, and atypical symptoms, leading to delayed recognition [55]. Outcomes in women are consistently worse, reflecting both biological vulnerability and systemic biases in healthcare delivery. Addressing these disparities requires both sex-specific prevention strategies and heightened awareness among clinicians.

Psychosocial and Socioeconomic Determinants

Unlike older CAD patients, young adults often face unique psychosocial challenges. Depression, chronic stress, and anxiety are disproportionately prevalent and independently increase cardiovascular risk [56]. Socioeconomic deprivation and limited access to care further worsen outcomes. Importantly, psychosocial stressors interact with biological mechanisms—altering cortisol rhythms, autonomic balance, and inflammatory pathways—to accelerate atherogenesis.

Implications for Clinical Practice

The findings have clear clinical implications:

1. Early screening: Young adults with family history or multiple risk factors should undergo lipid profiling, blood pressure monitoring, and lifestyle assessment.
2. Aggressive primary prevention: Smoking cessation, weight management, and dietary interventions are paramount.
3. Precision medicine approaches: Genetic testing for FH and elevated Lp(a) should be considered in high-risk individuals.
4. Rehabilitation and adherence programs: Tailored interventions are needed to address poor long-term adherence to medication and lifestyle modifications [57].

Public Health Perspective

From a public health standpoint, early-onset CAD is particularly devastating because it affects individuals in their most productive years. Policies must prioritize:

• School- and college-based prevention campaigns against smoking and obesity.
• Workplace wellness programs targeting sedentary behaviors.
• Community-based screening initiatives in high-risk regions, especially South Asia and the Middle East.
• Such interventions are not only medically necessary but also economically beneficial, as they reduce the long-term burden of disability and loss of productivity [58].

Research Gaps and Future Directions

Despite growing literature, several gaps remain:

• Lack of large, prospective, multicenter cohorts focused exclusively on early-onset CAD.
• Limited integration of genetic, epigenetic, and biomarker data into risk prediction models.
• Under-representation of women in clinical studies.
• Inadequate exploration of the impact of novel risk factors such as air pollution, sleep disorders, and emerging addictive behaviors.

Future research should adopt a multidisciplinary, precision medicine approach, integrating genomics, psychosocial determinants, and public health strategies to develop personalized prevention and treatment strategies.

A complex interplay of traditional, genetic, psychosocial, and environmental risk factors drives early-onset CAD in young adults. Its hallmark presentation as acute coronary syndromes with single-vessel, soft plaque disease distinguishes it from older-onset CAD. While short-term survival is favorable, long-term outcomes remain poor due to gaps in recurrence and secondary prevention. Regional disparities and sex differences further highlight the need for tailored, context-specific interventions. Future strategies must combine precision medicine with public health policies to effectively curb the rising burden of CAD in young adults.

Conclusion

Early-onset coronary artery disease (CAD) represents a growing global challenge, affecting young adults at the peak of their personal and professional productivity. This systematic review highlights the unique interplay of traditional risk factors such as smoking, dyslipidemia, and diabetes, alongside non-traditional determinants including genetic predispositions, psychosocial stressors, and substance use, in shaping premature CAD [59]. Distinct clinical and angiographic features—most notably the predominance of acute coronary syndromes, single-vessel involvement, and soft plaque morphology—set early-onset CAD apart from its later-onset counterpart. While short-term survival is favorable, long-term recurrence and poor adherence to secondary prevention remain persistent obstacles. Addressing this burden requires a two-pronged strategy: precision medicine approaches (genetic screening, biomarker-driven risk stratification, personalized therapy) and public health interventions (anti-smoking initiatives, early lifestyle modification, sex-specific preventive programs, and community-based awareness campaigns) [60]. Integrating these efforts into healthcare systems can transform premature CAD from a devastating individual and societal burden into a preventable, manageable condition.

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